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  1. #1
    Batman360's Avatar
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    liver support for injectables?

    I am doing a 12 week dbol / test cycle soon and I intend to use supps for liver support while on my cycle but I was wondering, do I need to support my liver only while taking oral or for both oral and injectable? How about for PCT, is Nolvadex harmful to the liver?

  2. #2
    Dizz28's Avatar
    Dizz28 is offline I reject your reality and substitute my own
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    Liver protector is not needed for Testosterone

    Nolvadex isn't harmful to the liver

  3. #3
    Batman360's Avatar
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    cool thanks! I can save some money. I'm doing Dbol for 4 weeks, how long after that could I stop using liver support supps?

  4. #4
    Mammon is offline Banned ~ Scammer
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    how long on the dbol ?

    ehh, answered that..
    i use liv-52 and NAC

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    johnnybigguns is offline Banned
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  6. #6
    lovex is offline Associate Member
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    what about clomid ???? is it harmful

  7. #7
    Batman360's Avatar
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    Quote Originally Posted by johnnybigguns View Post
    yep I was looking at that thread and calculated I need around $130 to support a 12 week cycle but since I'm only on dbol for 4 weeks I will only end up spending around $60-$80.

  8. #8
    Dizz28's Avatar
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    Quote Originally Posted by lovex View Post
    what about clomid ???? is it harmful
    It's known to cause visual disturbances and shifts in mood. I don't think long term effects are known

  9. #9
    Immortal Soldier's Avatar
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    Quote Originally Posted by Dizz28 View Post
    It's known to cause visual disturbances and shifts in mood. I don't think long term effects are known
    Dizz I would like your opinion on this (along with others such as Mammon):

    Clomiphene (Clomid) consists of two stereoisomers which possess radically different pharmacodynamics. Zuclomiphene has predominantly estrogenic effects and slow clearance while the enclomiphene isomer has predominately anti-estrogenic effects and quick clearance. (9) This creates a dichotomy between estrogen blockage and estrogen stimulation and an acute imbalance once Clomid administration is discontinued. Bodybuilders will often complain of “estrogenic rebound” after stopping Clomid, which could be attributed to the lingering estrogenic isomer zuclomiphene as the anti-estrogenic enclomiphene has long cleared the system. (Recently, enclomiphene has been isolated by the pharmaceutical company Repros, for use in Androxal™.)

    For all intents and purposes, tamoxifen is a superior SERM, simply for the fact that tamoxifen provides a purely anti-estrogenic isomer, whereas Clomid provides a mix of anti and pro estrogenic effects.

    In regards to the health consequences about to be listed, it can be safely assumed that Clomid will share similar detrimental effects as tamoxifen, since it shares the same triphenylethylene backbone and carcinogenic tendencies. (44,45,57,58)

    Liver cancer -

    Originally, tamoxifen was accepted as being non-toxic to human liver upon finding that tamoxifen did not cause noticeable liver damage (DNA adducts) during short-term test tube studies with human liver cells. (35,36)

    However, it became apparent that test tuberesearch was largely flawed due to the low rate of metabolism in such a superficial environment. (21) It was soon discovered that the hepatotoxic effects from tamoxifen are from the metabolism and buildup of the a-hydroxytamoxifen and N-desmethyltamoxifen metabolites, which would only appear in an in vivo environment. (15) Surely enough, the results from the original rat studies showing dramatic carcinogenic effects on the liver, 30-34,41 soon correlated with human data when researchers found the same type of liver DNA adducts in tamoxifen patients. (15, 28-34)

    More recent human research has reported tamoxifen treated women to have 3x the risk of developing fatty liver disease, which occurs as soon as 3 months into therapy at only 20mg/day. (24-26) In some cases, the disease lasts up to 3 years, despite cessation from tamoxifen therapy. Five and ten year follow-ups with patients on long term tamoxifen therapy shows cases of deadly hepatocellular carcinoma. (27-29)

    In 2002, a bizarre study examined the use of tamoxifen for hepatocellular carcinoma treatment in humans. It was assumed that since tamoxifen could inhibit proliferation of breast cancer, it could offer the same benefit for liver cancer. The devastating results could not have been further indicative of tamoxifen’s hepatotoxic nature, as the tamoxifen treatment significantly increased the rate of death, compared to the group not receiving tamoxifen. (14)

    Finally, in a case study reviewing tamoxifen induced liver disease; D.F Moffat et al made a profound statement –

    “hepatocellular carcinoma in tamoxifen treated patients may be under-reported since there may be reluctance to biopsy liver tumours which are assumed to be secondary carcinoma of the breast.”

    In other words, it appears that the liver carcinoma from a large number of breast cancer patients on tamoxifen therapy has been misdiagnosed as an infection from the breast cancer itself.
    (28)

    Although tamoxifen induced liver cancer may take years to manifest in a healthy male, its damaging effects could easily be exaggerated by other popular hepatotoxic drugs, such as 17aa oral steroids. (15)

    Prostate cancer -

    In 1996, the International Agency for Research on Cancer (IARC) concluded that tamoxifen clearly promotes uterine cancer in humans – at a standard 20mg/day dose. (16,23,42) This is due to tamoxifen acting as an estrogen agonist in the uterus, presumably from the 4-hydroxytamoxifen metabolite, which triggers abnormal growth of the uterus and the formation of cancer causing DNA adducts. (33, 40)

    Contrary to popular thought, these implications are quite scary for a male when we realize the male equivalent to the uterus is the prostate – which differentiates from the same embryonic cell line, shares the same oncogene, Bcl-2, and high concentration of estrogen receptors. In fact, there is no reason to assume that tamoxifen would not initiate the same cancerous growth in the prostate. (60-62) It is no wonder that tamoxifen failed as a treatment for prostate carcinoma. (43)

    Note: This same risk would be applicable to Clomid, which has also been linked to uterine cancer and ovarian hyper-stimulation. (18, 19, 57, 59)

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